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TOP 100 SECRETS 3
44. A woman with a history of a child with a neural tube defect should take 4 mg of folic
acid on a daily basis, but only 400 mcg daily is recommended for those without such a
history.
45. Advanced maternal age is associated with increased risks of chromosomal
abnormalities, first-trimester losses, and obstetric complications.
46. Pregnancy is a state of compensated respiratory alkalosis.
47. Plasma volume increases by as much as 45%, but red blood cell mass increases by
only 20-30%; this results in dilutional anemia.
48. During pregnancy, increased renal plasma flow and increased glomerular filtration rate
lead to decreased serum BUN and creatinine.
49. Pregnancy increases the risk of pyelonephritis due to anatomic changes and
decreased ureteral motility.
50. Cardiac output increases by 30-50% in pregnancy due to increases in heart rate and
stroke volume.
51. Labor and delivery can be a critical time for women with cardiac disease due to
dramatic fluctuations in hemodynamic and volume status.
52. Pregnancy is a hypercoagulable state due to increased clotting factors and venous
stasis.
53. Pulmonary embolism is the leading cause of maternal mortality in developed countries.
54. Group B streptococcal (GBS) infection is a cause of neonatal sepsis and carries a
high neonatal mortality and morbidity, especially in premature neonates. The CDC
recommends maternal screening via vaginal and rectal cultures in the late third
trimester and prophylaxis with antibiotics during labor for those who test positive.
55. All pregnant women should be screened for HIV.
56. Maternal parvovirus infection can cause fetal anemia, hydrops, and even intrauterine
demise.
57. Maternal systemic lupus erythematosus can cause congenital heart block, which is
nonreversible.
58. The risk of major and minor congenital anomalies in women on anticonvulsants is
4-6%, compared to the baseline population risk of 2-3%.
59. Although lithium has been associated with cardiac malformations—especially Ebstein’s
anomaly—the extent of the risk is unclear.
60. There is no safe level of alcohol consumption in pregnancy; the best advice is not to
drink alcohol at all.
61. The recommended weight gain in pregnancy for women of normal weight is 25-35
pounds.
62. Nausea and vomiting of pregnancy (NVP) usually resolves prior to 20 weeks gestation.
63. The only cure for preeclampsia is delivery.
64. Magnesium sulfate should be given to women with severe preeclampsia during labor
and for 24 hours after delivery to reduce the risk of seizures.
65. A nonfasting, 1-hour, 50-gm glucose challenge test is used to screen for gestational
diabetes; a fasting, 3-hour, 100-gm glucose tolerance test is then used to confirm the
diagnosis.
66. Gestational diabetes increases a woman’s risk of developing type 2 diabetes later
in life.
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4 TOP 100 SECRETS
67. in patients with insulin-dependent diabetes mellitus (IDDM), good glycemic control
should be achieved prior to conception in order to decrease the risk of congenital
malformations.
68. Although an increase in thyroid-binding globulin during pregnancy causes total
circulating T4 and T3 to increase, free levels are not changed.
69. The treatment of asthma in pregnancy is essentially the same as that for nonpregnant
women.
70. Women with genital herpes lesions or prodromal symptoms at the onset of labor
should deliver by cesarean delivery to prevent vertical transmission.
71. Placental abruption and stillbirth occur in 8% of pregnant cocaine users.
72. Postpartum blues occur in 50-80% of women, depression in 8-15%, and psychosis
in 1-2/1000.
73. Special considerations for general anesthesia in the pregnant woman include
aspiration risk, physiologic respiratory changes, hypercoagulability, and compression of
the inferior vena cava by the gravid uterus.
74. The initial evaluation of a pregnant trauma patient is the same for nonpregnant woman;
stabilize the mother before evaluating the fetus.
75. After 4 minutes of CPR in a pregnant woman, a perimortem cesarean should be
performed if there is no return of spontaneous circulation.
76. Preterm labor and delivery are common in multiple gestations; mean gestational
lengths are 35 weeks for twins, 33 weeks for triplets, and 31 weeks for quadruplets.
77. Twin-to-twin transfusion syndrome can occur in monozygotic pregnancies; it is caused
by an irregular distribution of placental vascular anastomosis between the fetuses.
78. Fetal hemolytic disease can occur when a pregnant woman produces antibodies
against fetal red blood cell antigens.
79. Rhogam is anti-D immunoglobulin; it is given to Rh-negative women at 28 weeks, at
any other time when there is risk for fetomaternal hemorrhage, and postpartum.
80. In the first trimester, gestational dating is determined by measuring the crown-rump
length. In the second and third trimesters, it is determined by measuring the biparietal
diameter, head circumference, femur length, and abdominal circumference.
81. Intrauterine growth restriction (IUGR) is generally defined as an estimated fetal weight
less than the tenth percentile; however, most adverse perinatal outcomes occur at
estimated weights less than the fifth percentile.
82. Fetal urine is the major source of amniotic fluid production after the first trimester, and
fetal swallowing is the major mode of resorption.
83. Although many cases of polyhydramnios are associated with maternal diabetes, the
majority of cases are idiopathic.
84. Human chorionic gonadotropin (HCG) is produced by the syncytiotrophoblast; it
maintains the production of progesterone by the corpus luteum in early pregnancy.
85. Abnormal placentation may occur over the internal cervical os (previa), be adherent to
the myometrium (accreta), invade into the myometrium (increta), or invade through the
myometrium (percreta).
86. Placenta previa classically presents as painless third-trimester vaginal bleeding;
placental abruption presents as painful vaginal bleeding.
87. Bed rest, pelvic rest, and/or restricted activity have not been proven to be effective in
reducing preterm delivery.
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TOP 100 SECRETS 5
88. Cervical cerclage is indicated for the treatment of cervical insufficency in singleton
pregnancies.
89. At the time of an exam, premature rupture of membranes (PROM) is confirmed by
pooling of fluid in the vaginal vault, a positive nitrazine test, and ferning of vaginal fluid
on a microscope slide.
90. External cephalic version is a technique where one or two people attempt to maneuver
a fetus from breech to cephalic presentation using directed pressure on the maternal
abdomen.
91. A non-stress test assesses fetal heart rate baseline, variability, and accelerations. It is
used to test for fetal well-being, and has a high negative predictive value.
92. Intrapartum fetal heart rate monitoring has been shown to decrease the number of
neonatal seizures, but it increases the number of cesarean deliveries without changing
the rate of long-term neurologic sequelae or cerebral palsy.
93. Fetal heart rate decelerations are defined by their relationship in time to contractions—
variable (caused by cord compression), early (head compression), and late
(uteroplacental insufficiency)
94. There are three stages of labor: onset of contractions to complete dilation, complete
dilation to delivery of fetus, and delivery of fetus to delivery of placenta.
95. There are seven cardinal movements of labor: engagement, descent, flexion, internal
rotation, extension, external rotation, and expulsion.
96. The most concerning complication of trial of labor after cesarean (TOLAC) is uterine
rupture; the type and number of previous uterine incision determines the degree of risk.
97. Unlike adults, neonatal resuscitation utilizes the “ABCs” (airway, breathing, and
circulation).
98. Postpartum hemorrhage is defined as blood loss > 500 mL for a vaginal delivery and >
1000 mL for a cesarean; the most common cause is uterine atony.
99. The most common complication of cesarean delivery is infection.
100. The most common cause of postpartum fever is endometritis, and the greatest risk
factor for this infection is cesarean delivery.
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7
1. At what ages do women begin and stop menstruating?
In the United States, menarche (the first menstruation) begins between the ages of 10 and 12 years
old; menopause (the last menstruation) can vary widely for each woman but generally occurs between
45 and 55 years of age.
2. What are the phases of the menstrual cycle, and which portions of the reproductive
system do they affect?
The menstrual cycle affects both the ovary and the endometrium, with two phases in each. Within the
ovary, the phases are follicular and luteal. Within the endometrium are proliferative and secretory phases.
In the ovary, the follicular phase matures the ovum in preparation for ovulation. The luteal phase
occurs after ovulation and is maintained by the corpus luteum; it is when the ovum moves through the
oviducts and prepares for fertilization and implantation.
In concert with the changes in the ovary, the endometrium matches the follicular phase of the
ovary with its own proliferative phase. During this time, the rising estrogen stimulates the endome-
trium to increase the number of glands, amount of stromal cells, and vasculature. The secretory phase
mirrors the luteal phase of the ovary and is mediated by the presence of progesterone; its purpose is
to prepare for implantation (Fig. 1-1).
3. What is the role of the hypothalamic-pituitary-ovarian (HPO) axis?
The HPO axis must be intact for the menstrual cycle to function properly; any disruption has an
impact. For example, improper maturation of gonadotropin-releasing hormone (GnRH) neurons at the
level of the hypothalamus can cause amenorrhea, as seen in Kallmann syndrome.
4. What are the two main hormones released by the pituitary gland during the
menstrual cycle?
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which are two glycoproteins that
have identical alpha-subunits. (This alpha-subunit is also shared by thyroid-stimulating hormone
[TSH] and human chorionic gonadotropin [hCG].)
5. When is the number of germ cells in the ovaries highest?
Primordial germ cells begin to form at 5 to 6 weeks of gestation, and they multiply to reach the
maximum amount of cells by 20 weeks (approximately 6 to 7 million per ovary). At birth, only approxi-
mately 2 million germ cells remain, as a result of atresia and apoptosis.
Women have approximately 300,000 germ cells per ovary at the time of puberty; by menopause,
fewer than 100,000 remain.
6. What are the two main layers of the endometrium?
The basal layer and the functional layer.
The basal layer overlies the myometrium and consists of glands and stroma that are not hor-
monally sensitive (i.e., they are not shed during menstruation).
The functional layer overlies the basal layer and is exposed to the uterine cavity. It is the site of
blastocyst implantation, it is sensitive to hormones, and it is shed during menstruation. During the
secretory phase, vacuoles within its glandular cells move from an intracellular to an intraluminal loca-
tion and are the reason for this phase’s name.
7. What is the mean duration of a menstrual cycle?
The mean duration is 28 ± 2 days. However, the normal range is between 21 and 35 days (28 ± 7 days). A
cycle shorter than 21 days is called polymenorrhea, and a cycle longer than days 35 is called oligomenorrhea.
8. When are the two most common times in a woman’s life for irregular menstrual
cycles to occur?
Two years after puberty and 3 years before menopause.
CHAPTER 1
THE MENSTRUAL CYCLE
Jacob Casey, MD, and Judy H. Chen, MD
I GENERAL GYNECOLOGY
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8 GENERAL GYNECOLOGY
9. What is a primordial follicle?
An oocyte arrested in the diplotene phase of meiosis I.
Primordial follicles are encompassed by a layer of granulosa cells that aid in the growth of the
follicle to become a primary (preantral) follicle and then a secondary (antral) follicle.
10. What are the three stages of the follicular phase?
1. Recruitment of antral follicles
2. Selection of a dominant follicle
3. Growth of the dominant follicle
11. What is the primary hormone responsible for follicular growth during the follicular
phase?
FSH, which provides the signal for further cell growth and rescues the follicle from atresia. An increase
in the FSH/LH ratio can be seen at the start of each follicular phase.
12. What two cell layers in the ovary are hormonally sensitive and important for the
maturation of a dominant follicle?
The granulosa cell layer and the theca cell layer.
The granulosa cell layer contains FSH receptors and is responsible for estrogen synthesis by
increasing the production of the enzyme aromatase.
The theca cell layer, which forms during follicular maturation, contains LH receptors and is
responsible for the production of androgens. Androgens from the theca cell layer diffuse back into the
granulosa cells and are converted into estrogen by aromatization.
Ovulation
Menstrual
phase
Proliferative
phase
Secretory phase
Luteal phaseFollicular phase
Estradiol
Progesterone
LH
FSH
048
Basalis
Functionalis
12
DAYS OF MENSTRUAL CYCLE
16 20 24 28
GONADOTROPINS
OVARIAN
STEROIDS
UTERINE
ENDOMETRIUM
OVARIAN
FUNCTION
Figure 1-1. Hormone levels during a normal menstrual cycle. (Modified from Gambone JC: Female reproductive
physiology. In Hacker NF, Gambone JC, Hobel CJ, eds. Hacker and Moore’s Essentials of Obstetrics and Gynecology.
5th ed. Philadelphia: Saunders, 2010.)
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THE MENSTRUAL CYCLE 9
13. How is a dominant follicle selected from a group of antral follicles, and at what
point in the cycle does this occur?
Although the exact mechanism is not known, dominant follicles have a greater sensitivity to FSH
compared with other follicles.
Dominant follicles are generally selected by day 6 to 9 of the menstrual cycle.
14. Approximately how many dominant follicles are formed in a woman’s lifetime?
Approximately 400.
15. What happens to the follicles not selected to become dominant?
They undergo apoptosis.
16. What is the LH surge, and what causes it?
The LH surge is an acute rise in LH that triggers ovulation. It is primarily driven by rising estrogen
production from the dominant follicle, which peaks approximately 24 to 36 hours before ovulation
(see Fig. 1-1).
17. When is ovulation most likely to occur?
Approximately 32 hours after luteinizing hormone (LH) starts to rise or approximately 16 hours after it
peaks (see Fig. 1-1).
18. How is the oocyte released from the ovary?
The LH surge induces an inflammatory-like response in which prostaglandins and proteases work to
break down the cell layers of the dominant follicle and allow for the oocyte to be released. Blood flow
to the follicle also increases during this time.
19. What happens to the oocyte on being released from the ovary?
The oocyte is now signaled to continue meiosis, in which it progresses from the diplotene stage of
meiosis I to arrest at the metaphase stage of meiosis II. At this point, the first polar body can be seen.
Meiosis II is completed only if fertilization occurs.
20. What does the remainder of the dominant follicle become after ovulation?
The remaining cell layers form a new structure called the corpus luteum and produce progesterone, a
key component of the luteal phase.
21. What are three major effects of progesterone during the luteal phase?
1. Negative feedback at the level of the hypothalamus decreases GnRH, which reduces secretion of
FSH and LH secretion.
2. Progesterone causes the hypothalamus to increase basal body temperature.
3. Progesterone increases the number of subnuclear vacuoles in the endometrium to prepare for
implantation.
22. When does the level of progesterone peak?
Approximately 8 days after the LH surge.
At this time the corpus luteum is still producing aromatase, which converts progesterone to
estrogen and causes a synchronous rise in both hormones (see Fig. 1-1).
23. How long does the luteal phase last?
The corpus luteum has a limited lifespan of 14 days; the start of the next menses therefore provides
information when ovulation occurred by counting backwards. However, there is increasing evidence
that there may be greater variability during this phase than previously believed.
24. What happens to the corpus luteum if fertilization occurs?
hCG produced by the blastocyst prevents degradation and allows for the continued production of
progesterone. Eventually, the placenta begins to synthesize enough progesterone to maintain the
pregnancy.
25. When should intercourse occur for the greatest chance of fertilization?
One to 2 days before ovulation.
Sperm can survive up to 5 days in the female genital tract, and the oocyte can survive up to
24 hours after ovulation.
26. When does implantation occur?
Implantation occurs 6 to 9 days after ovulation.
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10 GENERAL GYNECOLOGY
27. What triggers menstruation at the end of the cycle?
In the absence of implantation and subsequent hCG production, the functional layer of the endome-
trium is shed; endometrial glands and stroma are broken down by matrix metalloproteinases and
proteolytic enzymes.
28. How does cervical mucus change during the menstrual cycle?
During the follicular phase, estrogen causes thin, watery, or stringy mucus to facilitate sperm
transport. After ovulation, progesterone causes the mucus to thicken and act as a barrier to ascending
infection.
BiBliography
1. Hacker NF, Gambone JC, Hobel CJ. Hacker & Moore’s Essentials of Obstetrics and Gynecology. 5th ed. Philadelphia:
Saunders; 2009.
2. Lentz GM, Lobo RA, Gershenson DM, Katz VL. Comprehensive Gynecology. 6th ed. Philadelphia: Mosby; 2013.
3. Speroff L, Fritz MA. Clinical Gynecologic Endocrinology and Infertility. 7th ed. Philadelphia: Lippincott Williams & Wilkins;
2005.
KEY POINTS: MENSTRUAL CYCLE
1. FSH signals follicular recruitment and increases LH receptor expression.
2. LH midcycle surge predicts impending ovulation.
3. The lifespan of the corpus luteum requires tonic LH secretion or stimulation by hCG.
4. The phases of the menstrual cycle are as follows:
Ovary: follicular, ovulation, luteal
Endometrium: proliferative, secretory, menstrual
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11
1. What is premenstrual syndrome (PMS)?
Cyclic physical and behavioral symptoms that appear in the days preceding menses and interfere
with work or lifestyle, followed by a symptom-free interval. Symptoms typically occur during the luteal
phase of the menstrual cycle and abate by day 4 of menstruation.
2. What symptoms are associated with PMS?
Symptoms may be psychological, somatic, and/or behavioral. The most common symptoms are
irritability, anxiety, depression, mood swings, bloating, abdominal discomfort, weight gain, acne, breast
pain, headache, fatigue, and increased appetite with food cravings (particularly for sweets).
3. Do we know what causes PMS?
No. Numerous theories have been postulated, all of which have to do with various hormonal altera-
tions: ovarian hormones (estrogen and progesterone), fluids and electrolytes (aldosterone, renin and
angiotensin, and vasopressin), neurotransmitters (γ-aminobutyric acid [GABA] and serotonin), and
other hormones (endorphins, androgens, and glucocorticoids). The pathogenesis is likely related to
changes in gonadal steroid production during the luteal phase and their subsequent effect on neu-
rotransmitters such as GABA and serotonin in the central nervous system (CNS).
4. What is the incidence of PMS?
PMS affects 20% to 40% of women, with up to 20% experiencing moderate symptoms and up to 40%
having mild symptoms. From 2% to 10% of women are severely affected, thus making the incidence
of severe PMS approximately 6 in 1000 to 40 in 1000 women.
5. How is PMS diagnosed?
No specific tests or published diagnostic guidelines are available. However, the following criteria are
widely accepted among physicians:
1. Cyclic symptoms documented for at least two cycles, as a prospective diary of severity of
symptoms.
2. Symptoms occurring only during the luteal phase, approximately 2 weeks before menstruation.
3. Symptoms relieved by day 4 of menses.
6. What is premenstrual dysphoric disorder (PMDD)?
A severe form of premenstrual disorder affecting approximately 5% to 8% of women. Recognized by
the American Psychiatric Association and described in the Diagnostic and Statistical Manual of Mental
Disorders, fifth edition (DSM-5), the diagnosis requires five premenstrual symptoms with at least one
being a moderately to severely disabling affective symptom.
7. How is PMS treated?
Treatment is mainly directed toward the predominant bothersome symptoms. Education and under-
standing alone may be sufficient for many patients. Stress management and lifestyle changes
(e.g., weight loss, exercise, smoking cessation, and restriction of caffeine and alcohol consump-
tion) may improve symptoms, as well as calcium supplementation. Various medications have also
been shown to be effective and include selective serotonin reuptake inhibitors (SSRIs), alprazolam,
gonadotropin-releasing hormone (GnRH) agonists, oral contraceptive pills (OCPs), and spironolactone.
8. How is severe PMS or PMDD treated?
The American Congress of Obstetricians and Gynecologists (ACOG) currently recommends SSRIs
(fluoxetine and sertraline) as the drugs of choice for treatment of severe PMS or PMDD. Treatment can
be either continuous or confined to the luteal phase. The exact mechanism of symptom improvement
is unknown.
CHAPTER 2
PREMENSTRUAL SYNDROME
AND DYSMENORRHEA
Alin Lina Akopians, MD, PhD
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12 GENERAL GYNECOLOGY
9. Do GnRH agonists have a role in treatment?
Treatment with a GnRH agonist causes “medical menopause” and has been shown to improve PMS
symptoms. However, the resulting hypoestrogenic state has many unfavorable side effects, such as
depression, anxiety, irritability, vasomotor symptoms, vaginal dryness, and muscle aches. A long-term
risk of osteoporosis also exists.
10. Do OCPs have a role in treatment?
OCPs eliminate the hormonal fluctuations observed during normal menstrual cycles and have been
proven to be effective in treating PMDD. OCPs containing the progestogen drospirenone may help
ameliorate symptoms of water retention, bloating, weight gain, and breast tenderness because drospi-
renone is derived from an analogue of spironolactone and has both antiandrogenic and antimineralo-
corticoid properties.
11. Does spironolactone have a role in treatment?
The physical symptoms of fluid retention (e.g., weight gain and breast tenderness), as well as some
emotional symptoms, may be related to elevations in renin and angiotensin and in aldosterone and are
alleviated by spironolactone.
12. Can sterilization be used to treat PMS?
Sterilization by tubal ligation has not been shown to reduce PMS symptoms. In extraordinary cir-
cumstances, women with severe, debilitating disease can be treated with a total hysterectomy and
bilateral oophorectomy.
13. What is dysmenorrhea?
Pelvic pain associated with menstrual periods. It is classified as either primary or secondary, and the
pain is usually described as cramping. The pain can also be felt outside the pelvis and may manifest
as backaches, headaches, and extremity pain. Dysmenorrhea can be accompanied by a variety of
systemic symptoms such as lightheadedness, insomnia, nausea, vomiting, and diarrhea.
14. What is the difference between primary and secondary dysmenorrhea?
Primary dysmenorrhea is pain resulting from myometrial contraction during ovulatory cycles with no
associated identifiable pathologic process. Secondary dysmenorrhea is pain caused by other gyneco-
logic conditions. The most common conditions associated with secondary dysmenorrhea are uterine
leiomyomas, adenomyosis, and endometriosis.
15. What is the incidence of dysmenorrhea?
As many as 72% of women experience some discomfort associated with their menses. In a small
but significant percentage, symptoms are severe enough to interfere with daily activities or cause
absence from work or school. In adolescent girls, the prevalence of primary dysmenorrhea is thought
to be as high as 60% to 90%. Dysmenorrhea is less common and less severe in women who have
previously given birth.
16. Is dysmenorrhea considered to be a form of chronic pelvic pain?
No. Even though women with dysmenorrhea (particularly secondary dysmenorrhea) can have pelvic
symptoms between menstrual periods, dysmenorrhea is characterized by the onset or exacerbation of
symptoms in association with menses.
17. How is dysmenorrhea evaluated?
Primary dysmenorrhea is a clinical diagnosis. A thorough patient history is essential to rule out other
gynecologic or nongynecologic (e.g., urologic or gastrointestinal) causes of pelvic pain and connect
the timing or exacerbation of the symptoms to menstruation.
KEY POINTS: PREMENSTRUAL SYNDROME
1. PMS describes emotional and physical symptoms that occur at the same time in the menstrual
cycle each month.
2. Although no one cause of PMS has been established, treatments correlate with possible
causes, such as progesterone supplementation, SSRIs, and nonsteroidal antiinflammatory drugs
(NSAIDs).
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